Eckmann Christian R, Kraemer Brian, Wickens Marvin, Kimble Judith
Howard Hughes Medical Institute, 433 Babcock Drive, University of Wisconsin-Madison, Madison, WI 53706, USA.
Dev Cell. 2002 Nov;3(5):697-710. doi: 10.1016/s1534-5807(02)00322-2.
The FBF RNA binding proteins control multiple aspects of C. elegans germline development, including sex determination. FBF promotes the oocyte fate at the expense of spermatogenesis by binding a regulatory element in the fem-3 3'UTR and repressing this sex-determining gene. Here we report the discovery of GLD-3, a Bicaudal-C homolog and cytoplasmic protein that physically interacts with FBF. Using RNAi and a gld-3 deletion mutant, we show that GLD-3 promotes the sperm fate, a sex determination effect opposite to that of FBF. By epistasis analysis, GLD-3 acts upstream of FBF, and, in a yeast three-hybrid assay, GLD-3 interferes specifically with FBF binding to the fem-3 3'UTR. We propose that GLD-3 binds FBF and thereby inhibits its repression of target mRNAs.
FBF RNA结合蛋白控制秀丽隐杆线虫生殖系发育的多个方面,包括性别决定。FBF通过结合fem-3 3'UTR中的调控元件并抑制这个性别决定基因,以牺牲精子发生为代价促进卵母细胞命运。在此,我们报告了GLD-3的发现,它是一种双尾-C同源物和细胞质蛋白,与FBF发生物理相互作用。使用RNA干扰和gld-3缺失突变体,我们表明GLD-3促进精子命运,这是一种与FBF相反的性别决定效应。通过上位性分析,GLD-3在FBF的上游起作用,并且在酵母三杂交试验中,GLD-3特异性干扰FBF与fem-3 3'UTR的结合。我们提出GLD-3结合FBF,从而抑制其对靶mRNA的抑制作用。